I. Overview Spontaneous cerebral hemorrhage (sponteneouesintracerebralhemorrhage) is a non-trauma-induced bleeding in the brain parenchyma caused by spontaneous rupture of large and small intracranial arteries, veins and capillaries in adults. It can be divided into primary and secondary cerebral hemorrhage according to its cause. Primary cerebral hemorrhage accounts for about 80%-85% of cerebral hemorrhage, mainly including hypertensive cerebral hemorrhage (about 50%-70%), amyloid angiopathy cerebral hemorrhage (CAA, about 20%-30%) and unexplained cerebral hemorrhage (about 10%). Secondary cerebral hemorrhage mainly includes arteriovenous malformation, aneurysm, cavernous vascular malformation, arteriovenous fistula, Moyamoya disease (smog), hematological disease or coagulation dysfunction, intracranial tumor, vasculitis, hemorrhagic cerebral infarction, venous sinus thrombosis and adverse drug reactions. II. Diagnosis This consensus focuses on primary cerebral hemorrhage, and the diagnostic criteria are as follows. 1, There is a clear history of hypertension (hypertensive cerebral hemorrhage patients). 2, Imaging examination suggests typical bleeding sites, such as basal ganglia area, thalamus, ventricles, cerebellum, brainstem (patients with hypertensive cerebral hemorrhage), and lobes (patients with CAA). 3.Exclude coagulation disorders and hematological diseases. 4.CTA/MRA/MRV/DSA examination to exclude other cerebrovascular lesions (choose 1 or 2 kinds of examination). 5.Ultra-early (within 72h) or late enhanced MRI examination to exclude intracranial tumor. Pre-hospital and emergency room emergency management Pre-hospital emergency and emergency management are crucial to save lives and improve the prognosis of patients with cerebral hemorrhage. The process is as follows. 1. Pre-hospital emergency care: When performing emergency care at the scene of the attack, first observe the patient’s vital signs (record pulse, respiration, blood pressure) and the state of consciousness and pupil changes. Apply first-aid equipment to maintain the patient’s vital signs and quickly establish intravenous access. If the patient’s airway is not open, airway secretions should be cleared immediately; if the respiratory rate is abnormal and blood oxygen saturation drops rapidly, tracheal intubation and balloon-assisted breathing can be performed on site. If the patient’s blood pressure is too high or too low, use blood pressure-raising or blood pressure-lowering drugs to maintain the blood pressure within the basic normal range. If trauma occurs during the onset of the patient, attention should be paid to check for fractures, open injuries and closed organ bleeding, and simple treatment should be given according to the situation. After emergency on-site treatment, immediately transfer the patient to the nearest and qualified medical institution. Attention should be paid to keep the patient in lateral position at all times during the transfer to reduce bumps. 2.Emergency treatment: Upon arrival at the emergency department, the initial consultation should be conducted immediately. The patient’s vital signs need to be confirmed again, and strive to maintain stable vital signs. The importance of airway management should be highly emphasized during emergency resuscitation, and the airway should be kept unobstructed at all times. For patients with respiratory impairment or airway incompetence, airway intubation must be performed immediately, and emergency tracheotomy can be performed if intubation is difficult, and cricothyroid puncture, percutaneous tracheotomy or orthotracheotomy is recommended. Glasgow coma score (GCS) is performed according to the degree of consciousness impairment, physical activity impairment and speech impairment of the patient. With stable vital signs, a rapid cranial CT examination (bedside mobile CT examination is feasible for critically ill patients with conditions) is performed to determine whether there is cerebral hemorrhage and to clarify the size of the hematoma for subsequent triage. For patients with brain herniation, the emergency procedure should be more time-sensitive. 3. Triage to neurology/surgery or neurological intensive care unit (NICU): (1) Patients with small to medium intracranial hematoma and no obvious cranial hypertension can be temporarily treated conservatively, closely observed within 72 h of onset, and dynamically reexamined with cranial CT; (2) large intracranial hematoma (supratentorial hemorrhage >30 ml, subatentorial hemorrhage >10 ml, midline shift more than 5 mm, disappearance of cricoid and lateral fissure pools) Patients with cerebral hemorrhage, or with obstructive hydrocephalus, severe cranial hypertension or even brain herniation should be immediately triaged to neurosurgery for surgical treatment. If possible, patients with severe cerebral hemorrhage can be admitted to a special stroke unit or NICU. Non-surgical treatment Non-surgical treatment of cerebral hemorrhage includes intracranial hypertension treatment, blood pressure management, seizure control, hemostasis, application of anti-platelet drugs and prevention of deep vein thrombosis, temperature management, blood glucose management, nutritional support, neuroprotection, and complication prevention. 1.Treatment of intracranial hypertension: Active control of cerebral edema and reduction of intracranial pressure is an important part of the acute treatment of cerebral hemorrhage, and patients should be monitored for intracranial pressure if possible. Commonly used drugs to lower intracranial pressure include mannitol, glycerol fructose, human albumin, diuretics, etc. Mannitol in particular is the most widely used, the common dose is 1-4g/kg/d. When applying mannitol, attention should be paid to cerebral perfusion pressure and basic renal function. 2. Blood pressure management: A large number of studies have shown that hypertension at the time of hospitalization is associated with poor prognosis of cerebral hemorrhage. The Intensive Antihypertensive Phase 2 Trial in Acute Cerebral Hemorrhage (INTERACT2) study showed that the variability of systolic blood pressure is also a predictor of prognosis in patients with cerebral hemorrhage. Therefore, blood pressure should be lowered rapidly as early as possible after cerebral hemorrhage to reach the target value as soon as possible, but it is not advisable to lower blood pressure too low in a short period of time. Regarding the goal of BP lowering, recently published clinical trials such as the Intensive BP Lowering Trial in Acute Cerebral Hemorrhage (INTERACT), INTERACT2, Acute Treatment of Hypotension in Cerebral Hemorrhage Trial (ATACH), Acute Arterial Pressure Lowering Trial in Cerebral Hemorrhage (ADAPT), and Study of Acute Management of Stroke with Assessment and Improvement of Emergency Risk Factors in Cerebral Hemorrhage (SAMURAI) have been conducted for early intensive BP lowering (in lowering systolic blood pressure to below 140 mmHg within 6 h of onset and maintaining it for at least 24 h) has provided evidence. Among them, the INTERACT2 study confirmed the safety of early intensive BP lowering, suggesting that early intensive BP lowering improves the prognosis better than the previous BP lowering target of 180 mmHg. The study was included as primary evidence in the European Stroke Organization (ESO) Guidelines for the Management of Spontaneous Cerebral Hemorrhage (2014 edition), which recommends that “intensive BP lowering (systolic BP below 140 mmHg within 1 h) within 6 h of the onset of acute cerebral hemorrhage is safe and may be better than the 180 mmHg target. The American Heart Association/American Stroke Association (AHA/ASA) guidelines have also modified the target values for blood pressure management based on the aforementioned study. We refer to the AHA/ASA 2015 edition guidelines for BP target values. , and combined with the actual situation in China, it is recommended that (1) in patients with cerebral hemorrhage with systolic blood pressure between 150-220 mmHg and no contraindication to acute antihypertensive therapy, reduction of systolic blood pressure to 140 mmHg in the acute phase is safe (Class I, Level A evidence) and effective in improving functional outcome (Class IIa, Level B evidence). (2) In patients with cerebral hemorrhage with systolic blood pressure >220 mmHg, continuous intravenous medication with intensive blood pressure lowering and frequent blood pressure monitoring is reasonable (Class IIb, Level C evidence). However, in clinical practice, the decision of BP lowering target should be individualized according to the length of the patient’s hypertensive history, basal BP value, intracranial pressure and BP at admission. (3) In order to prevent excessive hypotension leading to cerebral perfusion pressure deficit, the daily hypotension can be lowered by 15% to 20% based on the hypertension at the time of human hospitalization, and this distribution stepwise hypotension method can be referred to. Rapid antihypertensive drugs are recommended to be given intravenously during the acute phase of cerebral hemorrhage, and drugs such as uradil, labetalol, esmolol hydrochloride, and enalapril can be chosen. Agitation is an important factor in the increase of peripheral blood pressure and intracranial pressure as well as the effect of antihypertensive treatment in patients with cerebral hemorrhage, and the cause of agitation should be actively sought and given timely treatment. Under the premise of ensuring the unobstructed airway, sedative treatment can be given appropriately, which can help to achieve the standard of blood pressure lowering. 3. Epilepsy prevention and control: There is not enough evidence to support prophylactic antiepileptic treatment, but many surgeons advocate that for supratentorial hematoma, perioperative prophylactic use of antiepileptic drugs can help reduce the incidence of epilepsy. For epileptiform seizures that reoccur 2-3 months after cerebral hemorrhage, long-term drug therapy is recommended as the conventional treatment for epilepsy. 4. Management of coagulation abnormalities: Coagulation abnormalities are both a cause of secondary cerebral hemorrhage and can also aggravate primary cerebral hemorrhage. For patients with cerebral hemorrhage, coagulation function should be routinely monitored. For those with coagulation factor deficiency and thrombocytopenia, coagulation factor or platelet replacement therapy can be given. In patients with cerebral hemorrhage triggered by oral anticoagulant drugs such as warfarin sodium tablets, such drugs should be discontinued and the international normalized ratio (INR) should be corrected as quickly as possible, such as vitamin K supplementation, fresh frozen plasma, and prothrombinogen complexes. Patients with cerebral hemorrhage are at high risk of thromboembolic disease. Intermittent air compression devices can be used on paralyzed limbs after vascular ultrasonography has ruled out venous embolism in the lower extremities, which has a preventive effect on the occurrence of deep vein embolism in cerebral hemorrhage. 5.Temperature management: Patients with cerebral hemorrhage may develop hyperthermia due to intracranial hematoma stimulation, infection or central causes. Cooling measures include treatment of infection, physical cooling and subcooling therapy. The goal of cooling is to control the body temperature below 38°C and try not to go below 35°C. Small sample studies have shown that subhypothermic treatment may prevent the expansion of perihematoma edema and complications and reduce the morbidity and mortality rate. 6. Glucose management: Regardless of whether there is previous diabetes, hyperglycemia at the time of admission for cerebral hemorrhage suggests higher morbidity and mortality and worse clinical prognosis. Excessively tight glycemic control may result in increased systemic or brain tissue hypoglycemic events and may increase the risk of death. At present, the optimal blood glucose value for patients with cerebral hemorrhage has not been determined, and blood glucose should be controlled within the normal range. 7. Nutritional support: Nutritional status is closely related to the clinical prognosis of patients. It is recommended that tools such as the Nutrition Risk Screening 2002 (NRS2002) be used to comprehensively assess the degree of nutritional risk of patients. Nutritional support should be given to those with nutritional risk as early as possible, which can be started within 24-48h after the onset of the disease, and in principle, enteral nutrition is preferred. If enteral nutrition cannot meet the demand, parenteral nutrition and transenteric nutrition can be considered alternately or simultaneously. 8.Neuroprotection: In the field of cerebral hemorrhage, a lot of literature reports that neuroprotective agents can help in disease recovery, however, there is still insufficient evidence of definite benefit of neuroprotective agents in the treatment of cerebral hemorrhage. 9. Complication prevention and control: After cerebral hemorrhage, various complications such as pulmonary infection, gastrointestinal bleeding and water-electrolyte disorders may occur, and patients may have a history of primary hypertension, diabetes mellitus, coronary heart disease and other chronic diseases, which may easily combine with heart, lung, kidney and other organ dysfunction. High attention should be paid to the prevention and treatment of complications. Lung infection is one of the most common complications of cerebral hemorrhage. Keeping the airway open and removing respiratory secretions in a timely manner can help reduce the occurrence of lung infection. Patients with hypertensive cerebral hemorrhage are prone to gastrointestinal bleeding. Prevention and treatment include routine application of histamine H2 receptor antagonists or proton pump inhibitors, avoidance or minimization of glucocorticoids, and early feeding or nasal nutrition. If the amount of gastrointestinal bleeding is large, blood and fluid transfusion should be given promptly, shock should be corrected, and if necessary, gastroscopic or surgical hemostasis should be used. The key to prevent electrolyte disturbance and renal insufficiency is reasonable rehydration and reasonable application of mannitol. Another common complication of the urinary system is infection, which is related to the longer duration of indwelling catheterization. Strict disinfection during indwelling catheterization can reduce the occurrence of infection. V. Surgical treatment The value of surgical treatment in cerebral hemorrhage is still the focus of controversy. The Surgical Treatment of Cerebral Hemorrhage Trial (STICH) series is the most influential study in the field of surgical treatment of cerebral hemorrhage. the STICHI study did not find that early (within 72 h of onset) surgical interventions benefited patients with supratentorial cerebral hemorrhage and only suggested that patients with superficial hematoma may benefit from surgery old J. The STICHII study for lobar hemorrhage reached the same conclusions as STICHI (iv) J. As a result, foreign guidelines, such as the AHA/ASA guidelines, only recommend surgical treatment for superficial intracerebral hematomas (within 1 cm of the cerebral cortex) and do not recommend surgery for deep hematomas. However, the existing clinical trials are flawed in terms of the severity of the patients enrolled, the indication for surgery, and the consistency of the level of surgery across participating centers, especially the fact that patients in the surgical treatment group are often sicker than those in the non-surgical treatment group, which may have influenced the judgment of the outcome, and therefore, the value of surgery in the treatment of cerebral hemorrhage cannot be dismissed on this basis. A recent Meta-analysis showed that patients with cerebral hemorrhage who underwent surgery within 8 h of onset, had a hematoma volume of 20-50 ml, a GCS score of 12-9, or were 50-69 years of age had a better prognosis for surgical treatment, and there was evidence of a more significant benefit of surgical treatment in those with superficial hematomas and no intraventricular hemorrhage. The main goal of surgical treatment is to promptly remove the hematoma, relieve cerebral compression, relieve severe intracranial hypertension and brain herniation, save the patient’s life, and minimize the secondary brain injury caused by hematoma compression. Surgery for deep intracerebral hematomas, represented by the basal ganglia region, has now become routine. It is important to note that in patients with severe cranial hypertension or even brain herniation with massive hematomas, the role of surgical treatment in saving lives is certain, even in the absence of high-level evidence-based medical evidence∞3. Chuan. In patients with moderate to small hematomas without significant cranial hypertension, the value of surgery remains to be further defined in randomized controlled clinical studies. Intracranial pressure monitoring is recommended for patients undergoing surgical treatment. Postoperative patients are recommended to review cranial CT at an appropriate time to assess the changes of postoperative hematoma; for patients with recurrent hematoma, the decision to operate again should be based on intracranial pressure and other conditions. 1. Basal ganglia hemorrhage: (1) Indications for surgery: Emergency surgery can be considered if one of the following manifestations is present: ① temporal lobe hook gyrus herniation; ② imaging with obvious intracranial hypertension manifestations (midline structure displacement more than 5mm; ipsilateral lateral ventricle compression occlusion more than 1/2; ipsilateral brain pool and brain sulcus blurred or disappeared); ③ actual measurement of intracranial pressure >25mmHg. (2) Surgical procedures and methods: ① bone flap craniotomy hematoma Removal: Although the bone flap craniotomy is slightly traumatic to the scalp and skull, it can completely remove the hematoma under direct vision, with reliable hemostasis and rapid decompression, and can also decide whether to perform debridement and decompression according to the patient’s condition and intracranial pressure changes, which is a more common and classic surgical approach. Generally, the temporal flap on the side of the lesion or the frontotemporal flap is opened, and the approach is via the middle temporal gyrus or the lateral fissure. In the transmedial temporal gyrus approach, a cerebral needle is used to puncture in the avascular or less vascular area to reach the hematoma cavity, and after confirming the presence of old blood, the middle temporal gyrus or insula cortex is cut open about 0.5-1.0 cm and separated into the hematoma cavity with a cerebral pressure plate; in the lateral fissure approach, the lateral fissure arachnoid is opened as much as possible to fully release the cerebrospinal fluid, and the frontal or temporal lobe is gently retracted to enter the hematoma cavity. Depending on the bleeding time and the hardness of the hematoma, the hematoma is gently aspirated with a small to medium-sized suction device. For individual hematomas that are tougher, ultrasonic laparoscopic aspiration or tumor forceps can be used to clip the hematoma. After complete removal of the hematoma, the hematoma cavity should be inspected. If there is active arterial bleeding, weak electrocoagulation can be used to stop the bleeding by accurate cautery, and general bleeding can be stopped by hemostatic material and cerebral cotton compression, and after determining that the hematoma is completely or basically cleared and the intracranial pressure is satisfactorily reduced, the bone flap should be returned and the skull should be closed layer by layer to end the operation. If the intraoperative brain tissue swelling is obvious and the intracranial pressure is not satisfied, decompression of the bone flap is feasible. Small bone window craniotomy for hematoma removal: Small bone window craniotomy causes little damage to the scalp and skull, and the procedure is relatively simple, and the hematoma can be removed quickly and the hemostasis is satisfactory under direct vision. A skin incision parallel to the lateral fissure projection line is made on the patient’s temporal bone, about 4-5 cm long, 1-2 holes are drilled in the temporal bone, a free bone flap of about 3 cm in diameter is milled with a milling cutter, and the dura is incised. The same can be done through the middle temporal gyrus or through the lateral fissure. After determining the site of the hematoma, the cerebral cortex is incised, and the incision is approximately 1 cm in length. A small cerebral pressure plate is used to gradually separate deeper into the hematoma cavity and gently aspirate the hematoma. After complete hemostasis and confirmation of low brain pressure and good brain pulsation, the dura was sutured, the skull bone flap was fixed, and all layers of the scalp were sutured layer by layer. (iii) Neuroendoscopic hematoma removal: A combination of rigid microscopy and stereotactic technique is used to remove the hematoma. The hematoma cavity is punctured under CT or B-ultrasound localization, and the hematoma is removed as much as possible without damaging the vessel wall, surrounding brain tissue and without causing new bleeding, but complete removal is not necessary to avoid causing new bleeding, i.e., it is sufficient to achieve the purpose of effectively reducing intracranial pressure. Stereotactic cone cranial hematoma aspiration: According to the CT localization of the hematoma site, stereotactic head frame positioning or scale positioning is used to avoid important blood vessels and functional areas, local infiltration anesthesia is selected, small straight incision (2 cm) is made to cut the scalp, the dura is cut after drilling, and the hematoma is punctured under direct vision using disposable intracranial hematoma crushing puncture needles or common suction devices, etc. The amount of hematoma is not limited for the first aspiration, and should be The first aspiration of the hematoma is not limited and should be aimed at decompression. The hematoma cavity should be left in a rigid drainage channel or drainage tube for continuous drainage for 3-5 d. (3) Key points of surgery: Regardless of the approach and procedure, new damage to the brain tissue should be avoided or minimized and the following precautions should be followed: ① Fine operation under microscope as much as possible; ② Special attention should be paid to protect the lateral fissure vein, middle cerebral artery and its branches and the unhemorrhaged doublestem artery; ③ No traction, or light traction with moderate traction; ④ Light suction and weak electrocoagulation, keeping the operation within the hematoma cavity to avoid damage to the brain tissue as much as possible. (4) Postoperative management: including reduction of intracranial pressure, blood pressure management, sedation, analgesia, prevention and treatment of intracranial and pulmonary infections and other infections, maintaining a stable internal environment, nutritional support, and prevention of epilepsy. The cranial CT should be routinely reviewed within 24h after surgery to understand the operation and to exclude postoperative rebleeding. It is recommended that for those with coagulation insufficiency or significant intraoperative bleeding, hemostatic drugs should be applied for a short period of time (within 24-48h) after surgery. 2. Thalamic hemorrhage: (1) Indication for surgery: refer to cerebral hemorrhage in the basal ganglia. (2) Surgical methods: ① various hematoma removal surgeries: refer to basal ganglia cerebral hemorrhage; ② ventricular borehole drainage: for patients with thalamic hemorrhage breaking into the ventricle, but small thalamic parenchymal hematoma, but obstructive hydrocephalus and secondary to obvious intracranial hypertension, generally perform lateral ventricular frontal horn borehole drainage. (3) Surgical points and postoperative management: refer to the basal ganglia hemorrhage. 3. Lobar hemorrhage: refer to basal ganglia hemorrhage. In patients with suspected CCA, special attention should be paid to intraoperative hemostasis. 4.Ventricular hemorrhage: (1)Surgical indications and methods: ①Small to moderate amount of hemorrhage, no obstruction | hydrocephalus, can be conservative treatment or continuous external drainage of the lumbar pool; ②Large amount of hemorrhage, more than 50% of the lateral ventricle, combined with obstructive hydrocephalus, external drainage of the ventricular borehole; ③Large amount of hemorrhage, more than 75% of the ventricle or complete ventricular cast, and obvious intracranial hypertension, external drainage of the ventricular borehole is feasible (3) If the bleeding volume is large, exceeds 75% of the ventricle or complete ventricular cast, and the intracranial hypertension is obvious, external ventricular drainage or craniotomy is feasible. (2) Surgical points and postoperative treatment: the same as basal ganglia hemorrhage. Cerebellar hemorrhage: (1) Indications for surgery: ① cerebellar hematoma >10ml; ② compression of the fourth ventricle, brainstem or complication of obstructive hydrocephalus. (2) Surgical method: subscapular median or paramedian approach, bone flap craniotomy for hematoma removal. (3) Surgical points and postoperative management: the same as the basal ganglia cerebral hemorrhage. 6. Contraindications to surgical treatment: (1) severe coagulation dysfunction; (2) confirmed brain death. The international multicenter Perindopril Prevention of Recurrent Stroke Study (PROGRESS), completed in 2001, confirmed that timely initiation of antihypertensive therapy in people who have had a stroke event, regardless of previous history of hypertension, is important for reducing stroke and other fatal or nonfatal vascular events, especially recurrent cerebral hemorrhage. The effect of timely initiation of antihypertensive therapy on reducing stroke and other fatal or nonfatal vascular events, especially cerebral hemorrhage recurrence, is clear. There are no studies that specifically address the optimal blood pressure target for reducing the risk of cerebral hemorrhage recurrence. Referring to the recommendations of the Joint National Committee on Prevention, Detection, Evaluation, and Treatment of Hypertension (JNC I8), reasonable blood pressure target values are <150/90 mmHg for patients ≥60 years of age, <140/90 mmHg for patients <60 years of age but ≥18 years of age, and <140/90 mmHg for patients with diabetes mellitus and chronic kidney disease. VII. Early rehabilitation After acute cerebral hemorrhage, early rehabilitation is necessary to improve the quality of life of patients and to improve the quality of life of patients. In order to improve the quality of life of patients and prevent recurrence. Generally speaking, rehabilitation treatment can be started after the patient's vital signs are stable. 3 months after the onset of the disease is the golden rehabilitation period, and 6 months is the effective rehabilitation period. The methods of rehabilitation treatment include: basic care, maintaining anti-spasticity position, position change, passive limb movement, bed turning training, bridging exercise, sitting training, standing training, walking training, Et normal life function training (ADL training), language function rehabilitation training, psychological rehabilitation treatment, etc. The new AHA/ASA statement on palliative care for stroke patients emphasizes that for all patients with severe or fatal stroke and their families, basic palliative care should be provided throughout the course of the disease and should be "tailored" to the patient's needs. Palliative care should be "tailor-made" for all patients with severe or fatal stroke and their families∞7|. Hospice care for cerebral haemorrhage in China is in its infancy, and there is a lack of scientific research, standardised palliative care systems and relevant research staff.